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VILIP-1 Downregulation in Non-Small Cell Lung Carcinomas: Mechanisms and Prediction of Survival

Overview of attention for article published in PLOS ONE, February 2008
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Mentioned by

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1 peer review site

Citations

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29 Dimensions

Readers on

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28 Mendeley
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Title
VILIP-1 Downregulation in Non-Small Cell Lung Carcinomas: Mechanisms and Prediction of Survival
Published in
PLOS ONE, February 2008
DOI 10.1371/journal.pone.0001698
Pubmed ID
Authors

Jian Fu, Kathryn Fong, Alfonso Bellacosa, Eric Ross, Sinoula Apostolou, Daniel E. Bassi, Fang Jin, Jirong Zhang, Paul Cairns, Inmaculada Ibañez de Caceres, Karl-Heinz Braunewell, Andres J. Klein-Szanto

Abstract

VILIP-1, a member of the neuronal Ca++ sensor protein family, acts as a tumor suppressor gene in an experimental animal model by inhibiting cell proliferation, adhesion and invasiveness of squamous cell carcinoma cells. Western Blot analysis of human tumor cells showed that VILIP-1 expression was undetectable in several types of human tumor cells, including 11 out of 12 non-small cell lung carcinoma (NSCLC) cell lines. The down-regulation of VILIP-1 was due to loss of VILIP-1 mRNA transcripts. Rearrangements, large gene deletions or mutations were not found. Hypermethylation of the VILIP-1 promoter played an important role in gene silencing. In most VILIP-1-silent cells the VILIP-1 promoter was methylated. In vitro methylation of the VILIP-1 promoter reduced its activity in a promoter-reporter assay. Transcriptional activity of endogenous VILIP-1 promoter was recovered by treatment with 5'-aza-2'-deoxycytidine (5'-Aza-dC). Trichostatin A (TSA), a histone deacetylase inhibitor, potently induced VILIP-1 expression, indicating that histone deacetylation is an additional mechanism of VILIP-1 silencing. TSA increased histone H3 and H4 acetylation in the region of the VILIP-1 promoter. Furthermore, statistical analysis of expression and promoter methylation (n = 150 primary NSCLC samples) showed a significant relationship between promoter methylation and protein expression downregulation as well as between survival and decreased or absent VILIP-1 expression in lung cancer tissues (p<0.0001). VILIP-1 expression is silenced by promoter hypermethylation and histone deacetylation in aggressive NSCLC cell lines and primary tumors and its clinical evaluation could have a role as a predictor of short-term survival in lung cancer patients.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
India 1 4%
France 1 4%
Unknown 26 93%

Demographic breakdown

Readers by professional status Count As %
Student > Master 5 18%
Researcher 4 14%
Student > Bachelor 2 7%
Student > Postgraduate 2 7%
Student > Ph. D. Student 2 7%
Other 4 14%
Unknown 9 32%
Readers by discipline Count As %
Medicine and Dentistry 6 21%
Agricultural and Biological Sciences 5 18%
Neuroscience 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Unspecified 1 4%
Other 3 11%
Unknown 10 36%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 28 March 2014.
All research outputs
#15,293,290
of 22,743,667 outputs
Outputs from PLOS ONE
#130,345
of 194,093 outputs
Outputs of similar age
#67,562
of 79,324 outputs
Outputs of similar age from PLOS ONE
#246
of 281 outputs
Altmetric has tracked 22,743,667 research outputs across all sources so far. This one is in the 22nd percentile – i.e., 22% of other outputs scored the same or lower than it.
So far Altmetric has tracked 194,093 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 15.1. This one is in the 24th percentile – i.e., 24% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 79,324 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 8th percentile – i.e., 8% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 281 others from the same source and published within six weeks on either side of this one. This one is in the 7th percentile – i.e., 7% of its contemporaries scored the same or lower than it.